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Durect Corporation osmotic minipump infusion
Rcan1 mediates AngII-induced neointima formation. The left femoral artery was wire injured and AngII was administrated by subcutaneous <t>minipump</t> infusion during 14 d. CsA administration commenced 24 h before treatment with AngII and continued throughout the AngII infusion period. (A) Representative Rcan1 immunostaining of left femoral artery cross sections from AngII-treated Rcan1 +/+ and Rcan1 −/− mice ( n = 5/group). Bar, 50 µm. (B) Images of femoral artery cross sections from AngII-treated Rcan1 +/+ and Rcan1 −/− mice stained with hematoxylin-eosin (HE), Van Gieson (VG), and Masson’s trichrome stains. Bar, 50 µm. Representative experiments are shown of 8–11 performed. (C) Quantification of the I/M ratio between groups. Data are means ± SEM. Mice per group were 8 Rcan1 +/+ AngII and 11 Rcan1 −/− AngII. *, P
Osmotic Minipump Infusion, supplied by Durect Corporation, used in various techniques. Bioz Stars score: 85/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 85 stars, based on 5 article reviews
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osmotic minipump infusion - by Bioz Stars, 2020-07
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1) Product Images from "Regulator of calcineurin 1 mediates pathological vascular wall remodeling"

Article Title: Regulator of calcineurin 1 mediates pathological vascular wall remodeling

Journal: The Journal of Experimental Medicine

doi: 10.1084/jem.20110503

Rcan1 mediates AngII-induced neointima formation. The left femoral artery was wire injured and AngII was administrated by subcutaneous minipump infusion during 14 d. CsA administration commenced 24 h before treatment with AngII and continued throughout the AngII infusion period. (A) Representative Rcan1 immunostaining of left femoral artery cross sections from AngII-treated Rcan1 +/+ and Rcan1 −/− mice ( n = 5/group). Bar, 50 µm. (B) Images of femoral artery cross sections from AngII-treated Rcan1 +/+ and Rcan1 −/− mice stained with hematoxylin-eosin (HE), Van Gieson (VG), and Masson’s trichrome stains. Bar, 50 µm. Representative experiments are shown of 8–11 performed. (C) Quantification of the I/M ratio between groups. Data are means ± SEM. Mice per group were 8 Rcan1 +/+ AngII and 11 Rcan1 −/− AngII. *, P
Figure Legend Snippet: Rcan1 mediates AngII-induced neointima formation. The left femoral artery was wire injured and AngII was administrated by subcutaneous minipump infusion during 14 d. CsA administration commenced 24 h before treatment with AngII and continued throughout the AngII infusion period. (A) Representative Rcan1 immunostaining of left femoral artery cross sections from AngII-treated Rcan1 +/+ and Rcan1 −/− mice ( n = 5/group). Bar, 50 µm. (B) Images of femoral artery cross sections from AngII-treated Rcan1 +/+ and Rcan1 −/− mice stained with hematoxylin-eosin (HE), Van Gieson (VG), and Masson’s trichrome stains. Bar, 50 µm. Representative experiments are shown of 8–11 performed. (C) Quantification of the I/M ratio between groups. Data are means ± SEM. Mice per group were 8 Rcan1 +/+ AngII and 11 Rcan1 −/− AngII. *, P

Techniques Used: Immunostaining, Mouse Assay, Staining

Rcan1 mediates AngII-induced AAA. Apoe −/− Rcan1 +/+ or Apoe −/− Rcan1 −/− mice were minipump infused with 1 µg/kg/min AngII for 28 d. (A) Rcan1 immunostaining (top) of abdominal aortic cross sections from saline- and AngII-treated Apoe −/− Rcan1 +/+ mice. IgG-staining serves as negative control. Rcan1-4 immunoblot of thoracic aorta (t) and the AAA segment of Apoe −/− Rcan1 +/+ mice are shown. Bar, 50 µm. (B) CD3, Mac3, SMA, and vimentin immunostaining of abdominal aortic cross sections from AngII-treated Apoe −/− Rcan1 +/+ mice. Bar, 50 µm. (A and B) Representative experiments are shown of four performed. (C) Abdominal aortas from AngII-treated mice. (D) Ultrasound images of abdominal aortas from AngII-infused animals. Transverse (top) and longitudinal (bottom) images were taken at the level of the suprarenal aorta. Yellow lines mark lumen boundary. (E) Suprarenal abdominal aorta cross sections stained with Masson’s trichrome. Bar, 100 µm. (C–E) Representative experiments are shown of 15–16 performed. (F and G) Maximum suprarenal abdominal aortic diameter (in millimeters) in AngII-treated mice measured at treatment start and treatment finish. (F) Triangles and squares represent individual mice and means ± SEM from Apoe −/− Rcan1 +/+ mice ( n = 16) and Apoe −/− Rcan1 −/− mice ( n = 15), respectively. *, P
Figure Legend Snippet: Rcan1 mediates AngII-induced AAA. Apoe −/− Rcan1 +/+ or Apoe −/− Rcan1 −/− mice were minipump infused with 1 µg/kg/min AngII for 28 d. (A) Rcan1 immunostaining (top) of abdominal aortic cross sections from saline- and AngII-treated Apoe −/− Rcan1 +/+ mice. IgG-staining serves as negative control. Rcan1-4 immunoblot of thoracic aorta (t) and the AAA segment of Apoe −/− Rcan1 +/+ mice are shown. Bar, 50 µm. (B) CD3, Mac3, SMA, and vimentin immunostaining of abdominal aortic cross sections from AngII-treated Apoe −/− Rcan1 +/+ mice. Bar, 50 µm. (A and B) Representative experiments are shown of four performed. (C) Abdominal aortas from AngII-treated mice. (D) Ultrasound images of abdominal aortas from AngII-infused animals. Transverse (top) and longitudinal (bottom) images were taken at the level of the suprarenal aorta. Yellow lines mark lumen boundary. (E) Suprarenal abdominal aorta cross sections stained with Masson’s trichrome. Bar, 100 µm. (C–E) Representative experiments are shown of 15–16 performed. (F and G) Maximum suprarenal abdominal aortic diameter (in millimeters) in AngII-treated mice measured at treatment start and treatment finish. (F) Triangles and squares represent individual mice and means ± SEM from Apoe −/− Rcan1 +/+ mice ( n = 16) and Apoe −/− Rcan1 −/− mice ( n = 15), respectively. *, P

Techniques Used: Mouse Assay, Immunostaining, Staining, Negative Control

Systemic delivery of LxVP lentivirus inhibits development of AngII-induced AAA. (A) Mice were inoculated with lentivirus expressing GFP-tagged LxVP or LxVPmutant 100 µl virus solution (10 11 particles in 100 µl) injected directly into the right jugular vein 1 mo before staining of aortic sections. (A) GFP immunostaining in aortic sections. IgG staining serves as a negative control. Bars: 100 µm (left); 50 µm (middle and right). A representative experiment is shown of six performed in independent mice. (B) Apoe −/− mice were inoculated with lentivirus expressing GFP-tagged LxVP or LxVPmutant 1 mo before minipump-infusion of 1 µg/kg/min AngII for 28 d. Maximum suprarenal abdominal aortic diameter (in millimeters) is shown. Triangles and squares represent individual mice and means ± SEM from six mice per condition, respectively. *, P
Figure Legend Snippet: Systemic delivery of LxVP lentivirus inhibits development of AngII-induced AAA. (A) Mice were inoculated with lentivirus expressing GFP-tagged LxVP or LxVPmutant 100 µl virus solution (10 11 particles in 100 µl) injected directly into the right jugular vein 1 mo before staining of aortic sections. (A) GFP immunostaining in aortic sections. IgG staining serves as a negative control. Bars: 100 µm (left); 50 µm (middle and right). A representative experiment is shown of six performed in independent mice. (B) Apoe −/− mice were inoculated with lentivirus expressing GFP-tagged LxVP or LxVPmutant 1 mo before minipump-infusion of 1 µg/kg/min AngII for 28 d. Maximum suprarenal abdominal aortic diameter (in millimeters) is shown. Triangles and squares represent individual mice and means ± SEM from six mice per condition, respectively. *, P

Techniques Used: Mouse Assay, Expressing, Injection, Staining, Immunostaining, Negative Control

CsA inhibits AngII-induced neointimal formation in a model of femoral artery injury. The left femoral artery was wire injured and AngII was administrated by subcutaneous minipump infusion during 14 d. CsA administration commenced 24 h before treatment with AngII and continued throughout the AngII infusion period. (A) Representative images of left femoral artery cross sections stained with hematoxylin-eosin (HE), Van Gieson (VG), and Masson’s trichrome (Masson). Bar, 50 µm. (B) Summary of morphometric data of the different treatment groups. Area data are shown in micrometers squared. Because the endothelial monolayer appeared as a line in the noninjured arteries, its area was considered to be 0, and the mean I/M ratio and percentage of stenosis were also 0. (C) Quantification of the ratio of the thickness of intima and media (I/M ratio) in the injured conditions shown in A. Data are means ± SEM. Numbers of mice per group were 7 saline, 13 AngII, 7 CsA+AngII, 5 CsA, and 10 noninjured. *, P
Figure Legend Snippet: CsA inhibits AngII-induced neointimal formation in a model of femoral artery injury. The left femoral artery was wire injured and AngII was administrated by subcutaneous minipump infusion during 14 d. CsA administration commenced 24 h before treatment with AngII and continued throughout the AngII infusion period. (A) Representative images of left femoral artery cross sections stained with hematoxylin-eosin (HE), Van Gieson (VG), and Masson’s trichrome (Masson). Bar, 50 µm. (B) Summary of morphometric data of the different treatment groups. Area data are shown in micrometers squared. Because the endothelial monolayer appeared as a line in the noninjured arteries, its area was considered to be 0, and the mean I/M ratio and percentage of stenosis were also 0. (C) Quantification of the ratio of the thickness of intima and media (I/M ratio) in the injured conditions shown in A. Data are means ± SEM. Numbers of mice per group were 7 saline, 13 AngII, 7 CsA+AngII, 5 CsA, and 10 noninjured. *, P

Techniques Used: Staining, Mouse Assay

CsA inhibits development of AngII-induced AAA. Apoe −/− mice were minipump infused with 5 mg/kg/d CsA, 1 d before commencing similar administration with saline or 1 µg/kg/min AngII for 28 d. (A) Representative abdominal aortas of Apoe −/− mice treated as indicated. (B) Representative high-frequency ultrasound (US) images of abdominal aortas. Transverse (top) and longitudinal (bottom) images were taken at the level of the suprarenal aorta. Yellow lines mark the lumen boundary. (C) Maximum suprarenal abdominal aortic diameter (in millimeters) measured from transverse US images. Triangles and squares represent individual mice and means ± SEM, respectively. Numbers of mice per group were 9 saline, 24 AngII, 9 CsA+AngII, and 7 CsA. *, P
Figure Legend Snippet: CsA inhibits development of AngII-induced AAA. Apoe −/− mice were minipump infused with 5 mg/kg/d CsA, 1 d before commencing similar administration with saline or 1 µg/kg/min AngII for 28 d. (A) Representative abdominal aortas of Apoe −/− mice treated as indicated. (B) Representative high-frequency ultrasound (US) images of abdominal aortas. Transverse (top) and longitudinal (bottom) images were taken at the level of the suprarenal aorta. Yellow lines mark the lumen boundary. (C) Maximum suprarenal abdominal aortic diameter (in millimeters) measured from transverse US images. Triangles and squares represent individual mice and means ± SEM, respectively. Numbers of mice per group were 9 saline, 24 AngII, 9 CsA+AngII, and 7 CsA. *, P

Techniques Used: Mouse Assay

AngII activates the CN–NFAT pathway in VSMCs in vivo. (A–C) Mice were inoculated with 5 mg/kg/d CsA, 10 mg/kg/d of the AngII type 1 receptor (AT 1 ) blocker losartan, or 30 mg/kg/d of the AngII type 2 receptor (AT 2 ) blocker PD123319 by subcutaneous osmotic minipump infusion for 24 h before similar administration of 1 µg/kg/min AngII for 1 h. Aortic sections from these mice were analyzed by Southwestern histochemistry with NFAT probe (A), hematoxylin-eosin (HE) staining (B), and Sp1 immunohistochemistry (C). Bars, 50 µm. (D) NFAT immunoblot in extracts from VSMCs stimulated with 1 µM AngII for 1 h after pretreatment as indicated (1 h) with 200 ng/ml CsA. Arrowheads indicate NFAT proteins with different degrees of phosphorylation. NFATc2 was tested in parallel protein extracts of Jurkat cells (JK). Representative experiments are shown of four to six performed.
Figure Legend Snippet: AngII activates the CN–NFAT pathway in VSMCs in vivo. (A–C) Mice were inoculated with 5 mg/kg/d CsA, 10 mg/kg/d of the AngII type 1 receptor (AT 1 ) blocker losartan, or 30 mg/kg/d of the AngII type 2 receptor (AT 2 ) blocker PD123319 by subcutaneous osmotic minipump infusion for 24 h before similar administration of 1 µg/kg/min AngII for 1 h. Aortic sections from these mice were analyzed by Southwestern histochemistry with NFAT probe (A), hematoxylin-eosin (HE) staining (B), and Sp1 immunohistochemistry (C). Bars, 50 µm. (D) NFAT immunoblot in extracts from VSMCs stimulated with 1 µM AngII for 1 h after pretreatment as indicated (1 h) with 200 ng/ml CsA. Arrowheads indicate NFAT proteins with different degrees of phosphorylation. NFATc2 was tested in parallel protein extracts of Jurkat cells (JK). Representative experiments are shown of four to six performed.

Techniques Used: In Vivo, Mouse Assay, Staining, Immunohistochemistry

2) Product Images from "Peripheral insulin-like growth factor-I produces antidepressant-like behavior and contributes to the effect of exercise"

Article Title: Peripheral insulin-like growth factor-I produces antidepressant-like behavior and contributes to the effect of exercise

Journal: Behavioural brain research

doi: 10.1016/j.bbr.2008.11.016

Peripheral IGF-I administration results in an antidepressant-like behavioral response in the forced-swim test (FST). IGF-I (50 ug/kg/day) was administered subcutaneously via osmotic minipump for 14 days. (A) IGF-I-treated mice showed decreased immobility in the FST compared with mice that received similar administration of vehicle. Student’s t -test, * p = 0.01, n = 9–10. (B) Antidepressant response to desipramine in the FST is shown for comparison. Desipramine (DMI) (20 mg/kg, i.p.) was administered in a single acute dose 30 min prior to test. Student’s t -test, * p = 0.01, n = 8/group. (C) Baseline locomotor activity of IGF-I-treated mice was not different from the activity of control mice. Horizontal distance traveled was measured by video tracking in standard mouse cages. Bars represent the mean±SEM for each experiment.
Figure Legend Snippet: Peripheral IGF-I administration results in an antidepressant-like behavioral response in the forced-swim test (FST). IGF-I (50 ug/kg/day) was administered subcutaneously via osmotic minipump for 14 days. (A) IGF-I-treated mice showed decreased immobility in the FST compared with mice that received similar administration of vehicle. Student’s t -test, * p = 0.01, n = 9–10. (B) Antidepressant response to desipramine in the FST is shown for comparison. Desipramine (DMI) (20 mg/kg, i.p.) was administered in a single acute dose 30 min prior to test. Student’s t -test, * p = 0.01, n = 8/group. (C) Baseline locomotor activity of IGF-I-treated mice was not different from the activity of control mice. Horizontal distance traveled was measured by video tracking in standard mouse cages. Bars represent the mean±SEM for each experiment.

Techniques Used: Mouse Assay, Activity Assay

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Mouse Assay:

Article Title: Regulator of calcineurin 1 mediates pathological vascular wall remodeling
Article Snippet: .. 2-mo-old mice were administered with various compounds by subcutaneous osmotic minipump infusion (Alzet Corp) as described previously ( ). .. AngII (Sigma-Aldrich) was administrated at 1 µg/kg/min during 28 d in AAA experiments and at 0.5 µg/kg/min during 14 d in femoral artery injury experiments.

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    Durect Corporation alzet osmotic minipump
    Alzet Osmotic Minipump, supplied by Durect Corporation, used in various techniques. Bioz Stars score: 92/100, based on 63 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/alzet osmotic minipump/product/Durect Corporation
    Average 92 stars, based on 63 article reviews
    Price from $9.99 to $1999.99
    alzet osmotic minipump - by Bioz Stars, 2020-07
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